Influence of hydration status on cardiovascular magnetic resonance myocardial T1 and T2 relaxation time assessment: an intraindividual study in healthy subjects.

BACKGROUND: Myocardial native T1 and T2 relaxation time mapping are sensitive to pathological increase of myocardial water content (e.g. myocardial edema). However, the influence of physiological hydration changes as a possible confounder of relaxation time assessment has not been studied. The purpose of this study was to evaluate, whether changes in myocardial water content due to dehydration and hydration might alter myocardial relaxation times in healthy subjects. METHODS: A total of 36 cardiovascular magnetic resonance (CMR) scans were performed in 12 healthy subjects (5 men, 25.8 ± 3.2 years). Subjects underwent three successive CMR scans: (1) baseline scan, (2) dehydration scan after 12 h of fasting (no food or water), (3) hydration scan after hydration. CMR scans were performed for the assessment of myocardial native T1 and T2 relaxation times and cardiac function. For multiple comparisons, repeated measures ANOVA or the Friedman test was used. RESULTS: There was no change in systolic blood pressure or left ventricular ejection fraction between CMR scans (P > 0.05, respectively). T1 relaxation times were significantly reduced with dehydration (987 ± 27 ms [baseline] vs. 968 ± 29 ms [dehydration] vs. 986 ± 28 ms [hydration]; P = 0.006). Similar results were observed for T2 relaxation times (52.9 ± 1.8 ms [baseline] vs. 51.5 ± 2.0 ms [dehydration] vs. 52.2 ± 1.9 ms [hydration]; P = 0.020). CONCLUSIONS: Dehydration may lead to significant alterations in relaxation times and thereby may influence precise, repeatable and comparable assessment of native T1 and T2 relaxation times. Hydration status should be recognized as new potential confounder of native T1 and T2 relaxation time assessment in clinical routine.

Parametric mapping using cardiovascular magnetic resonance for the differentiation of light chain amyloidosis and transthyretin-related amyloidosis.

AIMS: To evaluate different cardiovascular magnetic resonance (CMR) parameters for the differentiation of light chain amyloidosis (AL) and transthyretin-related amyloidosis (ATTR). METHODS AND RESULTS: In total, 75 patients, 53 with cardiac amyloidosis (20 patients with AL (66±12 years, 14 males [70%]) and 33 patients with ATTR (78±5 years, 28 males [88%])) were retrospectively analyzed regarding CMR parameters such as T1 and T2 mapping, extracellular volume (ECV), and late gadolinium enhancement (LGE) distribution patterns, and myocardial strain, and compared to a control cohort with other causes of left ventricular hypertrophy (LVH; 22 patients (53±16 years, 17 males [85%])). One way-ANOVA and receiver operating characteristic analysis were used for statistical analysis. ECV was the single best parameter to differentiate between cardiac amyloidosis and controls (area under the curve [AUC]: 0.97, 95% confidence intervals [CI]: 0.89-0.99, p<.0001, cutoff: >30%). T2 mapping was the best single parameter to differentiate between AL and ATTR amyloidosis (AL: 63±4 ms, ATTR: 58±2 ms, p<.001, AUC: 0.86, 95% CI: 0.74-0.94, cutoff: >61 ms). Subendocardial LGE was predominantly observed in AL patients (10/20 [50%] vs. 5/33 [15%]; p=.002). Transmural LGE was predominantly observed in ATTR patients (23/33 [70%] vs. 2/20 [10%]; p<.001). The diagnostic performance of T2 mapping to differentiate between AL and ATTR amyloidosis was further increased with the inclusion of LGE patterns (AUC: 0.96, 95% CI: 0.86-0.99]; p=.05). CONCLUSION: ECV differentiates cardiac amyloidosis from other causes of LVH. T2 mapping combined with LGE differentiates AL from ATTR amyloidosis with high accuracy on a patient level.